results indicate that a dysfunction of the neurosteroid system might be operative in BPD in spite of unchanged DBI plasma levels.

There was a significant difference in the rs2276596 polymorphism C/A allele frequency of the DBI gene (P < 0.0001) between alcoholics and healthy controls.

Acyl-CoA binding protein and epidermal barrier function. [review]

Endogenous potentiation of GABAergic synaptic transmission and responses to GABA uncaging in the thalamic reticular nucleus is absent in mice in which DBI is deleted and mice in which benzodiazepine binding to alpha3 subunit-containing GABAARs is disrupted.

A human preadipocyte cell line SGBS (zeige GPC3 Antikörper) is well suited to examine differential expression of the Acyl-CoA binding protein (ACBP) during adipogenesis.

Mice with conditional targeting of the Acbp gene in the epidermis recapitulate this phenotype, whereas generation of an artificial epidermal barrier during gland development reverses the phenotype

This study demonistrated that a novel role for ACBP in brain lipid metabolism.

Acyl-CoA binding protein and epidermal barrier function. [review]

ACBP is required for production of VLC-FFA for stratum corneum and for maintaining normal epidermal barrier function

It was concluded that acyl-CoA binding protein via aquaporin 3 (zeige AQP3 Antikörper) is necessary for intact urine concentrating ability through efflux over the basolateral membrane of the collecting duct.

Diazepam Binding Inhibitor (DBI) Antigen-Profil

Protein Überblick

This gene encodes diazepam binding inhibitor, a protein that is regulated by hormones and is involved in lipid metabolism and the displacement of beta-carbolines and benzodiazepines, which modulate signal transduction at type A gamma-aminobutyric acid receptors located in brain synapses. The protein is conserved from yeast to mammals, with the most highly conserved domain consisting of seven contiguous residues that constitute the hydrophobic binding site for medium- and long-chain acyl-Coenzyme A esters. Diazepam binding inhibitor is also known to mediate the feedback regulation of pancreatic secretion and the postprandial release of cholecystokinin, in addition to its role as a mediator in corticotropin-dependent adrenal steroidogenesis. Three pseudogenes located on chromosomes 6, 8 and 16 have been identified. Multiple transcript variants encoding different isoforms have been described for this gene.